The question of whether pathogenesis of the “early” and “late” onset cases is similar enough to qualify as a single disease was previously raised although not conclusively settled. Interestingly, debate on this issue has not kept pace with advancing knowledge about the molecular, biochemical and clinical underpinnings of tangle-and-plaque dementias. Since the question of whether both forms of AD share a common pathogenesis could profoundly impact diagnostic and treatment development efforts, it seems worthwhile to revisit this debate. (Link)

Early-onset (familial) Alzheimer’s disease, which is far less prevalent than late-onset (sporadic) AD, has been an attractive subject for study because of its clearer inheritance pattern. Researchers reasoned that it would be easier to understand the molecular underpinnings of the disease after they had a genetic handle on the players.

I’m intrigued by the idea that this eminently reasonable course of study might have given the field a molecular understanding of a disease that affects a minority of sufferers, and whose etiology is somewhat (or even quite) distinct from the one that costs us the oft-quoted millions of minds.

A separate review that also addresses the heterogeneity of the sporadic disease appears this week in the Lancet.